ArticleNature immunology2019
Macrophages, rather than DCs, are responsible for inflammasome activity in the GM-CSF BMDC model.
Article in Nature immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed, 101 citations in OpenAlex.
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- 5-Aminolevulinic Acid (5-ALA) Plays an Important Role in the Function of Innate Immune Cells.Inflammation · 2025Article
- Natriuretic peptides as novel regulators of dendritic cells-mediated inflammation.Cellular and molecular life sciences : CMLS · 2025Article
- High intensity forced ultrasound-driven ferroptosis as a strategy for anti-tumor immune priming.Acta pharmaceutica Sinica. B · 2025Article
- Bidirectional Communication Between the Innate and Adaptive Immune Systems.Annual review of immunology · 2025Review
- The impact of STING signaling on myeloid cells highlights macrophages as the major player in controllingFrontiers in immunology · 2025Article
- The coral pathogen Vibrio coralliilyticus uses a T6SS to secrete a group of novel anti-eukaryotic effectors that contribute to virulence.PLoS biology · 2024Article
- ADP as a novel stimulus for NLRP3-inflammasome activation in mice fails to translate to humans.Purinergic signalling · 2024Article
- Dysregulated dendritic cells in sepsis: functional impairment and regulated cell death.Cellular & molecular biology letters · 2024Review
- A pH/ROS dual-responsive system for effective chemoimmunotherapy against melanomaActa pharmaceutica Sinica. B · 2024Article
- Review
- High Intensity Focused Ultrasound-Driven Nanomotor for Effective Ferroptosis-Immunotherapy of TNBC.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- NLRP3 inflammasome-a likely target for the treatment of immunologic conjunctivitis: A protocol for systematic review and meta-analysis.PloS one · 2024Article
- A1 is induced by pathogen ligands to limit myeloid cell death and NLRP3 inflammasome activation.EMBO reports · 2023Article
- Lipid metabolism in dendritic cell biology.Immunological reviews · 2023Review
- A proinflammatory long noncoding RNA Lncenc1 regulates inflammasome activation in macrophage.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- A Preliminary Study of Mild Heat Stress on Inflammasome Activation in Murine Macrophages.Cells · 2023Article
- NOD2 in monocytes negatively regulates macrophage development through TNFalpha.Frontiers in immunology · 2023Article
- The role and mechanisms of gram-negative bacterial outer membrane vesicles in inflammatory diseases.Frontiers in immunology · 2023Review
1 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammasomes are one of the most important mechanisms for innate immune defense against microbial infection but are also known to drive various inflammatory disorders via processing and release of the cytokine IL-1β. As research into the regulation and effects of inflammasomes in disease has rapidly expanded, a variety of cell types, including dendritic cells (DCs), have been suggested to be inflammasome competent. Here we describe a major fault in the widely used DC-inflammasome model of bone marrow-derived dendritic cells (BMDCs) generated with the cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF). We found that among GM-CSF bone marrow-derived cell populations, monocyte-derived macrophages, rather than BMDCs, were responsible for inflammasome activation and IL-1β secretion. Therefore, GM-CSF bone marrow-derived cells should not be used to draw conclusions about DC-dependent inflammasome biology, although they remain a useful tool for analysis of inflammasome responses in monocytes-macrophages.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.